Int. J.
Cancer: 78, 707–711 (1998)
r 1998 Wiley-Liss, Inc.
ALCOHOL AND OTHER BEVERAGE USE AND PROSTATE CANCER RISK AMONG
CANADIAN MEN
Meera G. JAIN1*, Gregory T. HISLOP2, Geoffrey R. HOWE3, J. David BURCH3 and Parviz GHADIRIAN4
1Cancer Epidemiology Unit, Department of Public Health Sciences, University of Toronto, Toronto, Canada
2Division of Epidemiology and Cancer Prevention, BC Cancer Agency, Vancouver, Canada
3Division of Epidemiology, School of Public Health, Columbia University, New York, NY, USA
4Research Unit in Epidemiology, CHUM, Hotel Dieu Montreal, Montreal, Canada
There are very few large scale studies that have examined
the association of prostate cancer with alcohol and other
beverages. This relationship was examined in a case-control
study conducted in 3 geographical areas of Canada [Metropoli-
tan Toronto (Ontario), Montreal (Quebec), and Vancouver
(British Columbia)] with 617 incident cases and 637 popula-
tion controls. Complete history of beverage intake was
assessed by a personal interview with reference to a 1-year
period prior to diagnosis or interview. In age- and energy-
adjusted models for all centers combined, the odds ratio (OR)
for the highest quintile of total alcohol intake was 0.89. For
alcoholic beverages separately, it was 0.68 for the highest
tertile of beer, 1.12 for wine and 0.86 for liquor. The decreas-
ing trend was significant for beer intake. The results were
only significant for British Columbia out of all the 3 centers
studied. Whereas coffee and cola intake was not associated
with prostate cancer, a decrease in risk was observed with tea
intake of more than 500 g per day (OR 0.70). Our results do
not support a positive association between total alcohol,
coffee and prostate cancer. Int. J. Cancer 78:707–711, 1998.
r 1998 Wiley-Liss, Inc.
Prostate cancer accounts for the highest number of incident
cancers among men in Canada and second only to lung cancer in
terms of deaths (National Cancer Institute of Canada, 1998). A
biologically plausible protective role for alcohol in prostate carcino-
genesis has been hypothesized from reports that alcohol may
increase metabolic clearance of testosterone (Gordon et al., 1976).
There are very few epidemiological studies that have examined the
relationship between alcohol intake and the risk of prostate cancer.
Wynder et al. (1971), in a comprehensive review of the epidemiol-
ogy of prostate cancer and also based on interviews with 217 cases
and 200 hospital controls, reported no association of this cancer
with alcohol intake. Of the other case-control studies that assessed
effects of alcohol (Hayes et al., 1996; Mishina et al., 1985; Ross et
al., 1987; Tavani et al., 1994; Walker et al., 1992; Yu et al., 1988),
only one (Hayes et al., 1996) has reported a substantial increase in
risk with alcoholic drinks, in Black and White Americans, whereas
cohort studies reported no association (Hiatt et al., 1994; Severson
et al., 1989). A cohort study of American men reported that
increased consumption of beer was weakly associated with an
increased risk of prostate cancer; smoking-adjusted relative risks
for ex-users and current drinkers of beer were 1.7 and 1.2,
respectively (Hsing et al., 1990). Another cohort study of men in
Japan found a relative risk of 2.7 for non-smoker men who drank
alcohol daily (Hirayama, 1992).
The study by Hayes et al. (1996) is the first large-scale study
(988 cases and 1,336 controls) of prostate cancer and the findings
of a positive association emphasize the need to confirm these
results in similar scale studies. Our study presents this opportunity
to test the association in a large sample of 1,253 men. In addition,
we examined the effect of caffeine-containing beverages as risk
factors for prostate cancer. Of the various reports on coffee intake
and prostate cancer (Fincham et al., 1990; Hsing et al., 1990;
Jacobson et al., 1986; Nomura et al., 1986; Severson et al., 1989;
Slattery and West, 1993; Talamini et al., 1992), one cohort study
reported a weak decreasing effect with increased intake of coffee
(Jacobson et al., 1986). The common occurrence of this cancer and
the fact that alcohol and other caffeine-containing beverage con-
Publication of the International Union Against Cancer
Publication de l’Union Internationale Contre le Cancer
sumption is a common exposure, implies that even a moderate
change in risk may be of public health significance.
MATERIAL AND METHODS
Our case-control study was conducted in 3 geographical areas of
Canada [Metropolitan Toronto (Ontario), Montreal (Quebec) and
Vancouver (British Columbia)], to examine the relationship be-
tween various dietary factors, including alcohol and other bever-
ages, and risk of prostate cancer. In each center, the study was
conducted according to a common protocol, which included the use
of questionnaires with a core set of identical questions. The
sampling frames for the controls differed in the 3 centers, but all
were essentially population-based. The total study population
consisted of 617 cases (187 in Ontario, 229 in Quebec and 201 in
British Columbia) and 636 controls (207 in Ontario, 230 in Quebec
and 199 in British Columbia).
Cases
Men were eligible for inclusion in the study as cases if they had a
recent, histologically confirmed diagnosis of adenocarcinoma of
the prostate.
Ontario cases. All cases notified to the Ontario Cancer Registry
(OCR) between April 1990 and April 1992, and resident in
metropolitan Toronto and surrounding areas (York, Peel and
Halton), were included in our study. Pathology reports were
received at the OCR within 6 months of diagnosis for more than
90% of cases occurring in Ontario. A random sample of 750 was
selected from a total of 4,227 cases notified to the OCR during this
period. Of the 367 eligible cases from these, for whom doctor’s
permission was obtained, 207 were interviewed (56.4%), 74
refused (20.2%) and the remaining 86 cases were not interviewed
for various reasons. For this analysis, 17 more cases were deleted
as their diagnosis date was prior to the study period and another 3
who had reported extremely high caloric intake of greater than
10,000 kcal per day.
Quebec cases. During 1989–1993, 881 patients were identified
through admission offices of 5 major francophone teaching hospi-
tals in Montreal. Of the 361 eligible cases from these, 232 (64.2%)
were interviewed for the study, 3 interviewed cases were later
excluded because of incorrect diagnosis and lack of sufficient data,
56 (15.5%) declined to be interviewed, 31 were not contacted
because of incorrect address and 40 were not interviewed because
of termination of the study.
British Columbia cases. Men were eligible for inclusion as cases
if they had had a recent, histologically confirmed diagnosis of
Grant sponsor: National Cancer Institute of Canada.
*Correspondence to: Cancer Epidemiology Unit, Department of Public
Health Sciences, 308–12 Queen’s Park Crescent West, University of
Toronto, Toronto, Ontario, Canada M5S 1A8. Fax: (416) 978–1490.
E-mail: meera.jain@utoronto.ca
Received 13 May 1998; Revised 29 June 1998
708 JAIN ET AL
adenocarcinoma of the prostate notified to the British Columbia
Cancer Registry between 1 January 1989 and 31 December 1991. A
total of 6,183 cases were notified to the registry during the study
period, and attempts were made to recruit a random sample of those
eligible. For this purpose, random number tables were used each
month to select a sufficient number of cases to ensure that the total
sample size required for the study would be reached during the
3-year recruitment period, with the proviso that about one-half of
those selected should be under the age of 70, and one-half aged 70
or older. Of the 229 cases approached in all, 201 (87.8%) were
interviewed, 5 had died, 3 were too ill to participate, 4 had moved
and 16 refused to participate.
Controls
Ontario controls. Potential controls were identified by randomly
selecting men from assessment lists maintained by the Ontario
Ministry of Finance. These lists contain the age, gender and address
of all residents and are updated twice a year. The lists are organized
by census division, and therefore it was possible to select potential
controls from the same geographic areas as the cases. For the
purposes of the present study, the Ministry of Finance provided a
list consisting of the names of a sample of men residing in these
areas, stratified by 5-year age group, and with frequency distribu-
tion by age corresponding to the expected age distribution of the
cases. Attempts were made to recruit one control per case. In
Toronto, 733 subjects were approached, of whom 109 did not speak
English, 58 had moved out of the study area and 41 had died. Of the
remaining 525 subjects, 207 (39.4%) were interviewed, 27 (5.1%)
were either too ill or senile, 97 (18.5%) could not be contacted and
194 (37.0%) refused to participate.
Quebec controls. Population-based controls matched for age
(⫾5 years) and place of residence were selected by a modified
random-digit dialing (RDD) method. A page from the telephone
directory was selected randomly from the sampling frame and the
names and addresses of 10 individuals were chosen with the same
first 3 telephone digits as the patient. Attempts were made to recruit
one control per case. Of the 711 controls selected by RDD, 462
(65%) were eligible and the remaining 249 (35%) were non-
eligible (did not answer, refused to participate before the study was
explained, wrong age, non-French-Canadians, etc.). Therefore, a
total of 231 controls or 50% of the eligible controls were
interviewed (1 later deleted because of insufficient information).
British Columbia controls. Potential controls were identified by
randomly selecting men from rosters maintained by the Medical
Services Plan of British Columbia, which covers almost the entire
population of the province. Controls were frequency matched on a
5-year age group to the age distribution of the cases. A total of 262
subjects were approached, of whom 9 had moved and 14 had died.
Of the remaining 239 subjects, 199 (83.3%) were interviewed, 1
had incomplete information, 3 were too ill to participate and 36
refused to do so.
Procedures
Potential cases and controls in all 3 study areas were initially
contacted by a letter and subsequently by telephone. Those with
unlisted numbers were not included because participation rates are
generally low in such subjects. Several phone calls were made on
different days and times, until a contact was made or a failure to
contact was established by the interviewer. All interviews were
conducted at the subjects’ home by trained interviewers, except in
Quebec where interviews for hospitalized patients and controls
were also conducted in hospitals. The interviewers used a struc-
tured questionnaire on dietary and non-dietary factors. The non-
dietary component of the questionnaire elicited information on
demographic characteristics, height, weight at various times during
life, physical activity patterns, personal and medical history,
smoking, frequency of use of the medical system and history of
rectal examination.
A validated, quantitative diet history was used to obtain esti-
mates of daily intake of alcohol and a great majority of foods found
in the Canadian diet (Jain et al., 1996). The diet history contained
questions concerning seasonality, usual frequency and usual amount
of consumption of various foods. Quantification was achieved by
the use of physical volumetric food models. In reporting intake,
cases were asked to address their usual intake to the 1-year
prediagnosis period, while controls were asked to address it to the 1
year prior to the interview date. Daily intakes of alcohol and other
nutrients were calculated using the Agriculture Handbook 8 of the
U.S. Department of Agriculture and expanded for Canadian foods
(Watt and Merril, 1972). Validation of alcohol and other beverages
was performed using data from a previously conducted validation
study on a random sample of 203 men and women in Toronto (Jain
et al., 1996). The Pearson’s correlation coefficients between
beverage intake in grams per day from the diet history compared
with 7-day food records were: 0.80 for beer, 0.55 for wine , 0.75 for
liquor, 0.68 for coffee, 0.68 for tea and 0.44 for cola intake. The
amount of alcohol for various drinks was calculated as: 3.6% for
beer, 11.5% for wines and sherry and 37.9% for liquor or spirits, so
that we calculated approximately 12.6 g of alcohol for each 350-ml
drink of beer, 13.8 g per 120-ml glass of wine and 17.1 g per 45-ml
drink of whiskey.
Statistical analysis
Odds ratios (OR) and 95% confidence intervals (CI) for the
association between alcohol and risk of prostate cancer were
obtained from unconditional logistic regression models (Breslow
and Day, 1980). The analyses were conducted for each center
separately, and for the 3 centers combined. All models were
adjusted for age by including age as a continuous variable. Results
were also adjusted for total energy intake because alcohol and all
beverages were positively associated with total energy. The interac-
tion between cigarette smoking and alcohol intake was also
examined to rule out any confounding by smoking, which has been
found to be weakly associated with prostate cancer in the present
data set (Rohan et al., 1997). Additional adjustment for educational
level, family history of prostate cancer, history of benign prostatic
hypertrophy, Quetelet’s index, energy intake and retinol intake had
little impact on the point estimates and p values, and therefore the
results of simpler models are presented here. Tests for trend (on 1
degree of freedom) were performed over exposed categories only
by fitting categorized indicator variables as continuous variables.
RESULTS
The analyses included 1,253 subjects, 617 cases and 636
controls from all 3 centers. The means for various characteristics
for cases were: age, 69.8 years (SD 7.3); body weight, 79.3 kg;
daily energy intake, 2,951 kcal; total alcohol, 19.1 g; alcohol from
beer, 6.5 g; alcohol from wine, 5.0 g; alcohol from liquor, 7.7 g;
coffee, 509.3 ml; tea, 284.3 ml; and cola, 62.0 ml. The values for
controls were: age, 69.9 years (SD 7.3); body weight, 78.5 kg; daily
energy intake, 2,731 kcal; total alcohol, 16.9 g; alcohol from beer,
5.3 g; alcohol from wine, 5.3 g; alcohol from liquor, 7.4 g; coffee,
461.3 ml; tea, 317.5 ml; and cola, 72.0 ml. Nearly 72% of cases and
75% of controls reported alcohol consumption.
Statistically significant positive associations were observed in
the present data set with a family history of prostate cancer in
first-degree relatives, whereas a history of rectal examination in the
last 5 years and vasectomy was negatively associated with prostate
cancer risk. High intakes of total energy, saturated fat, polyunsatu-
rated fats and retinol were positively associated. These have been
described in detail in previous publications (Ghadirian et al., 1996;
Rohan et al., 1995). These were considered as confounders in the
analyses. The relation of alcohol intake with these putative factors
is shown in Table I. For these analyses, alcohol consumption was
classified into 3 categories (non-drinkers, ⬍ 20 and ⱖ 20 g/day).
Consumers of ⱖ 20 g/day of alcohol were less likely to be over 70
years of age, to have a family history of prostate cancer than
non-drinkers and to have high retinol intakes. They were more
 BEVERAGE INTAKE AND PROSTATE CANCER RISK 709

likely to have higher education, a history of vasectomy, smoked 0.77–2.33). The adjusted ORs for prostate cancer in men reporting
cigarettes and higher energy and fat intakes. alcohol from beer of over 9 g per day were significantly decreased
The overall risk of prostate cancer with alcohol consumption or (combined and British Columbia area). There was some decrease in
with any of the specific beverages, without any adjusting variables, risk with alcohol from liquor of over 15 g, but in general no
was not significantly different from unity. The p values were all particular association was observed with beer, wine or liquor. The
greater than 0.05. When risks were examined by level of daily total ORs for the highest level of intake, for all centers combined, were:
alcohol consumption while simultaneously adjusting for age and 0.68 (0.49–0.94) for beer, 1.12 (0.80–1.55) for wine and 0.86
total energy intake, a decreasing, non-significant association was (0.63–1.18) for liquor. There was no evidence of an interaction
found with increasing levels of intake for all study centers between cigarette smoking and alcohol in these data (p value ⫽
combined and for British Columbia and Ontario (Table II). The 0.23 for the interaction term).
ORs for the highest level of intake with reference to the lowest For non-alcoholic beverages considered for these analyses
intake of total alcohol were 0.89 (0.64–1.25) for all centers (Table III), there was no association with coffee intake with the
combined, 0.57 (0.31–1.04) for British Columbia and 0.78 (0.43– exception of a decreasing risk for Ontario, but no significant trend.
1.42) for Ontario. For Quebec, the trend was toward a non- A slightly decreased risk was seen with tea intake of more than 500
significant increasing risk (OR ⫽ 1.34, 95% confidence interval g (approximately 2 cups/day) for the total sample and for Ontario.
Cola did not show any association. The ORs for the highest level of
TABLE I – RELATIONSHIP OF ALCOHOL CONSUMPTION TO POTENTIAL
intake of each of these beverages were: 0.97 (0.65–1.44) for coffee,
CONFOUNDERS IN CONTROL SUBJECTS, CANADA 1989–1993 0.70 (0.50–0.99) for tea and 0.79 (0.53–1.17) for cola.
Percent with characteristic by
Additional adjustment for smoking (ever/never), educational
alcohol intake categories level, family history of prostate cancer, history of benign prostatic
Characteristic
None ⬍20 g/day ⱖ20 g/day hypertrophy, Quetelet’s index, energy intake and retinol intake had
(n ⫽ 160) (n ⫽ 282) (n ⫽ 194) little impact on the point estimates and p values of all the
beverages.
Age ⱖ70 64.4 58.2 43.3
⬎12 years of education 28.8 47.5 55.2
Had benign prostatic hypertrophy 9.4 9.6 8.2 DISCUSSION
Had vasectomy 8.1 11.3 11.9
Positive family history of prostate 5.6 5.3 4.1 We found no increased risk of prostate cancer with alcohol
cancer intake in this Canadian population. Our results are similar to some
Ever married 91.8 97.2 95.4 previously reported studies on alcohol and prostate cancer (Hiatt et
Ever smoked cigarettes 69.4 72.6 85.1
Quetelet’s index (⬎27)1,2 43.1 40.8 39.2 al., 1994; Mishina et al., 1985; Ross et al., 1987; Severson et al.,
Energy intake (⬎3,245 kcal/day)1 21.3 23.4 30.9 1989; Tavani et al., 1994; Walker et al., 1992; Wynder, 1971; Yu et
Saturated fat intake 22.5 24.1 28.6 al., 1988) and do not support reports of an increased risk associated
(⬎42.24 g/day)1 with beer drinking (Hsing et al., 1990) and alcohol (Hayes et al.,
Polyunsaturated fat intake 18.1 27.3 27.3 1996). In fact, there was a decreasing trend with beer drinking in
(⬎18.81 g/day)1 our data, showing a dose–response relationship for the total study
Retinol intake (⬍1,101 IU/day)1 29.4 24.1 22.7 population and for British Columbia subjects, the findings support-
1Highest quartile for Quetelet’s index, energy, saturated fat, polyun- ing the suggestion by Gordon et al. (1976) that alcohol may exert a
saturated fat; lowest for retinol.–2Quetelet’s index: weight, kg/height, protective role through testosterone clearance. The beverage intake
m.2 information in our study related to intakes in the 1 year before the

TABLE II – RISK OF PROSTATE CANCER BY ALCOHOL INTAKE AND STUDY CENTER, CANADA 1989–1993

All centers British Columbia Ontario Quebec

Cases/ OR (95% CI) Cases/ OR (95% CI) Cases/ OR (95% CI) Cases/ OR (95% CI)
controls controls controls controls

Number of subjects 617/636 201/199 187/207 229/230

Alcohol intake (g/day)
Total alcohol
01 175/160 1.00 55/42 1.00 57/53 1.00 63/65 1.00
⬎0–⬍10 168/189 0.80 (0.59–1.08) 59/59 0.71 (0.41–1.23) 42/52 0.71 (0.41–1.25) 67/78 0.89 (0.55–1.44)
10–⬍20 82/93 0.80 (0.55–1.15) 24/26 0.71 (0.35–1.41) 34/42 0.70 (0.34–1.27) 24/25 0.99 (0.51–1.91)
20–⬍30 57/68 0.75 (0.50–1.14) 21/26 0.61 (0.30–1.25) 14/20 0.57 (0.26–1.26) 22/22 1.04 (0.52–2.06)
ⱖ30 135/126 0.89 (0.64–1.25) 42/46 0.57 (0.31–1.04) 40/40 0.78 (0.43–1.42) 53/40 1.34 (0.77–2.33)
p-value for trend 0.51 0.07 0.35 0.23
Alcohol from beer
01 333/315 1.00 110/87 1.00 109/118 1.00 114/110 1.00
⬎0–9 189/205 0.83 (0.64–1.07) 62/78 0.58 (0.37–0.91) 52/50 1.00 (0.62–1.61) 75/77 0.94 (0.62–1.42)
ⱖ10 95/116 0.68 (0.49–0.94) 29/34 0.56 (0.31–1.01) 26/39 0.58 (0.32–1.04) 40/43 0.86 (0.51–1.44)
p-value for trend 0.01 0.02 0.11 0.56
Alcohol from wine
01 323/314 1.00 101/98 1.00 117/110 1.00 105/106 1.00
⬎0–9 193/236 0.77 (0.60–0.99) 73/75 0.91 (0.56–1.40) 40/64 0.54 (0.33–0.88) 80/97 0.83 (0.55–1.24)
ⱖ10 101/86 1.12 (0.80–1.55) 27/26 0.98 (0.53–1.84) 30/33 0.78 (0.44–1.39) 44/27 1.64 (0.95–2.85)
p-value for trend 0.81 0.83 0.81 0.26
Alcohol from liquor
01 331/329 1.00 99/83 1.00 100/106 1.00 132/140 1.00
⬎0–15 190/201 0.93 (0.73–1.20) 67/65 0.86 (0.54–1.36) 53/67 0.78 (0.49–1.24) 70/69 1.08 (0.72–1.63)
ⱖ16 96/106 0.86 (0.63–1.18) 35/51 0.54 (0.32–0.92) 34/34 0.98 (0.56–1.71) 27/21 1.32 (0.71–2.47)
p-value for trend 0.33 0.03 0.69 0.39
OR, odds ratio; CI, confidence interval. OR and CI adjusted for age (continuous) and total energy intake.–1Reference category (non-drinkers of
specific beverage).
710 JAIN ET AL

TABLE III – RISK OF PROSTATE CANCER BY OTHER BEVERAGE INTAKE AND STUDY CENTER, CANADA 1989–1993

All centers British Columbia Ontario Quebec

Cases/ Cases/ Cases/ Cases/
controls OR (95% CI) controls OR (95% CI) controls OR (95% CI) controls OR (95% CI)

Number of subjects 617/636 201/199 187/207 229/230

Beverage intake (g/day)
Coffee
01 70/65 1.00 16/18 1.00 31/21 1.00 23/26 1.00
⬎0–500 342/378 0.84 (0.58–1.22) 95/107 1.00 (0.48–2.09) 96/121 0.53 (0.28–0.98) 151/150 1.16 (0.63–2.12)
⬎500 205/193 0.97 (0.65–1.44) 90/74 1.40 (0.66–2.98) 60/65 0.57 (0.30–1.11) 55/54 1.15 (0.58–2.28)
p-value for trend 0.84 0.16 0.23 0.75
Tea
01 183/168 1.00 46/47 1.00 60/49 1.00 77/72 1.00
⬎0–500 335/344 0.89 (0.69–1.16) 109/104 1.07 (0.65–1.75) 92/108 0.70 (0.44–1.13) 134/132 0.95 (0.64–1.42)
⬎500 99/124 0.70 (0.50–0.99) 46/48 0.91 (0.51–1.64) 35/50 0.54 (0.30–0.98) 18/26 0.61 (0.31–1.22)
p-value for trend 0.05 0.77 0.04 0.27
Cola
01 407/397 1.00 143/146 1.00 129/130 1.00 135/121 1.00
⬎0–200 154/176 0.83 (0.64–1.08) 50/45 1.18 (0.73–1.79) 39/51 0.73 (0.45–1.19) 65/80 0.72 (0.48–1.09)
⬎200 56/63 0.79 (0.53–1.17) 8/8 0.88 (0.31–2.44) 19/26 0.71 (0.37–1.35) 29/29 0.85 (0.47–1.52)
p-value for trend 0.10 0.76 0.16 0.26
Abbreviations: OR, odds ratio; CI, confidence interval. OR and CI adjusted for age (continuous) and total energy intake.–1Reference category
(non-drinkers of specific beverage).

diagnosis of cancer and whether the presence of a subclinical
disease at that stage resulted in any altered behavior in terms of
drinking is difficult to assess. We had asked the subjects to report of
any changes in diet lasting over 6 months and changes in alcohol or
beverage intake was not reported frequently enough to warrant a
separate analysis. Only 9% of the subjects reported ever being on a
special diet over their lifetime. With regard to non-differential
measurement errors, risks may be underestimated due to these
errors, but in view of the relatively high correlation coefficients
observed in the validity study (data not shown), it is unlikely that
these biases will be substantial. It has been speculated that alcohol
might result in prostate cancer indirectly through dietary effects,
including nutrient displacement, malabsorption and its effect on
pathology of liver (Lieber et al., 1979). However, supportive
evidence from cirrhotic subjects is lacking (Glantz, 1964). Alcohol
or its metabolites (IARC, 1988), acetaldehyde, could also have
direct effects on metabolism or on cytochrome and enzyme
systems.
Our results showed no increased risk of prostate cancer with
coffee or cola intake; however, a decreased risk was observed with
tea intake of over 500 g per day for all subjects combined and for
Ontario. Tea is a rich source of certain antioxidants called
phytochemicals, in particular, polyphenols such as tannins and
catechin, and glucosinolates. If caffeine or theobromine intake
should promote carcinogenesis, it is not evident from this study.
The average consumption of these substances in Canada is 240
mg/day: 55% as coffee, 32% as tea and 7% as soft drinks (Toronto’s
Addiction and Mental Health Services Corporation). Coffee, as the
major source of caffeine, does not exhibit any effect in our study.
The effect of tea needs to be investigated in future studies of
prostate cancer.
Adjustment for confounding variables such as education, smok-
ing status, family history of disease, history of benign prostatic
hypertrophy and rectal examination in the past 5 years did not
change the point estimates or interpretations appreciably. Addi-
tional adjustment for other dietary variables, which were reported
to be of some significance for prostate cancer risk, did not alter
results.
ACKNOWLEDGEMENTS
The study was partly supported by the National Cancer Institute
of Canada. We thank Dr. T. Rohan for facilitating the retrieval of
data for this study.

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